Angiotensin converting enzyme 2 （ACE2） is a new member of renin-angiotensin system found recently. It counterbalances the effects of angiotensin converting enzyme （ACE）, hydrolyzes angiotensin Ⅱ to generate angio...Angiotensin converting enzyme 2 （ACE2） is a new member of renin-angiotensin system found recently. It counterbalances the effects of angiotensin converting enzyme （ACE）, hydrolyzes angiotensin Ⅱ to generate angiotensin-（1-7） and hydrolyzes angiotensin Ⅰ to produce angiotensin-（1-9）. Angiotensin-（1-9） can be hydrolyzed by ACE to form angiotensin-（1-7）, and angiotensin-（1-7） counteracts the effects of angiotensin Ⅱ in many aspects. Bradykinin or atrial natriuretic factor or substance P are not the substrates of ACE2, and ACE2 hydrolyzes the metabolites of bradykinin such as des-Arg9-BK and des-Arg10-kallidin, and also the dynorphin A, one of the opium peptides. ACE2 is not inhibited by angiotensin-converting enzyme inhibitor （ACEI）. Recent studies demonstrate that ACE2 is a functional receptor of SARS coronavirus. To elucidate the mechanisms of cardiovascular diseases and other disease such as SARS, further investigations in ACE2 are needed.展开更多
目的研究血管紧张素(Ang)家族新成员Ang-(1-9)对动脉粥样硬化中关键黏附分子血管细胞黏附分子1(VCAM-1)表达的作用及调控机制。方法在体外培养人脐静脉内皮细胞,给予相应刺激进行分组:对照组;AngⅡ为实验1组;Ang-(1-9)为实验2组;AngⅡ+A...目的研究血管紧张素(Ang)家族新成员Ang-(1-9)对动脉粥样硬化中关键黏附分子血管细胞黏附分子1(VCAM-1)表达的作用及调控机制。方法在体外培养人脐静脉内皮细胞,给予相应刺激进行分组:对照组;AngⅡ为实验1组;Ang-(1-9)为实验2组;AngⅡ+Ang-(1-9)为实验3组;AngⅡ+氯沙坦为实验4组;AngⅡ+Ang-(1-9)+PD123319为实验5组。采用RT-PCR及流式细胞仪检测VCAM-1 mRNA及蛋白表达,荧光素酶报告基因检测法测定VCAM-1启动子活性,酶联免疫吸附法测定NF-κB细胞核内水平,细胞免疫荧光观察NF-κB细胞核内转移情况。结果与对照组比较,实验1组VCAM-1 mRNA和蛋白表达明显增加(2.61±0.05 vs 1.00±0.00,146.35±1.81 vs 11.17±0.52,P<0.05);与实验1组比较,实验3组和实验4组VCAM-1 mRNA和蛋白表达明显减少,差异有统计学意义(P<0.05)。与对照组比较,实验1组VCAM-1启动子活性和NF-κB在细胞核内表达明显增加,差异有统计学意义(P<0.05);与实验1组比较,实验3组VCAM-1启动子活性和NF-κB在细胞核内表达明显降低,差异有统计学意义(P<0.05);与实验3组比较,实验5组VCAM-1启动子活性和NF-κB在细胞核内表达明显增加,差异有统计学意义(P<0.05)。结论Ang-(1-9)对VCAM-1的抑制作用有助于为动脉粥样硬化疾病的防治提供新思路。展开更多
文摘Angiotensin converting enzyme 2 （ACE2） is a new member of renin-angiotensin system found recently. It counterbalances the effects of angiotensin converting enzyme （ACE）, hydrolyzes angiotensin Ⅱ to generate angiotensin-（1-7） and hydrolyzes angiotensin Ⅰ to produce angiotensin-（1-9）. Angiotensin-（1-9） can be hydrolyzed by ACE to form angiotensin-（1-7）, and angiotensin-（1-7） counteracts the effects of angiotensin Ⅱ in many aspects. Bradykinin or atrial natriuretic factor or substance P are not the substrates of ACE2, and ACE2 hydrolyzes the metabolites of bradykinin such as des-Arg9-BK and des-Arg10-kallidin, and also the dynorphin A, one of the opium peptides. ACE2 is not inhibited by angiotensin-converting enzyme inhibitor （ACEI）. Recent studies demonstrate that ACE2 is a functional receptor of SARS coronavirus. To elucidate the mechanisms of cardiovascular diseases and other disease such as SARS, further investigations in ACE2 are needed.
文摘目的研究血管紧张素(Ang)家族新成员Ang-(1-9)对动脉粥样硬化中关键黏附分子血管细胞黏附分子1(VCAM-1)表达的作用及调控机制。方法在体外培养人脐静脉内皮细胞,给予相应刺激进行分组:对照组;AngⅡ为实验1组;Ang-(1-9)为实验2组;AngⅡ+Ang-(1-9)为实验3组;AngⅡ+氯沙坦为实验4组;AngⅡ+Ang-(1-9)+PD123319为实验5组。采用RT-PCR及流式细胞仪检测VCAM-1 mRNA及蛋白表达,荧光素酶报告基因检测法测定VCAM-1启动子活性,酶联免疫吸附法测定NF-κB细胞核内水平,细胞免疫荧光观察NF-κB细胞核内转移情况。结果与对照组比较,实验1组VCAM-1 mRNA和蛋白表达明显增加(2.61±0.05 vs 1.00±0.00,146.35±1.81 vs 11.17±0.52,P<0.05);与实验1组比较,实验3组和实验4组VCAM-1 mRNA和蛋白表达明显减少,差异有统计学意义(P<0.05)。与对照组比较,实验1组VCAM-1启动子活性和NF-κB在细胞核内表达明显增加,差异有统计学意义(P<0.05);与实验1组比较,实验3组VCAM-1启动子活性和NF-κB在细胞核内表达明显降低,差异有统计学意义(P<0.05);与实验3组比较,实验5组VCAM-1启动子活性和NF-κB在细胞核内表达明显增加,差异有统计学意义(P<0.05)。结论Ang-(1-9)对VCAM-1的抑制作用有助于为动脉粥样硬化疾病的防治提供新思路。
